@article{63c4aa6c2a864d3f89f95acfc115a67b,
title = "Coupling of Rigor Mortis and Intestinal Necrosis during C. elegans Organismal Death",
abstract = " Organismal death is a process of systemic collapse whose mechanisms are less well understood than those of cell death. We previously reported that death in C. elegans is accompanied by a calcium-propagated wave of intestinal necrosis, marked by a wave of blue autofluorescence (death fluorescence). Here, we describe another feature of organismal death, a wave of body wall muscle contraction, or death contraction (DC). This phenomenon is accompanied by a wave of intramuscular Ca 2+ release and, subsequently, of intestinal necrosis. Correlation of directions of the DC and intestinal necrosis waves implies coupling of these death processes. Long-lived insulin/IGF-1-signaling mutants show reduced DC and delayed intestinal necrosis, suggesting possible resistance to organismal death. DC resembles mammalian rigor mortis, a postmortem necrosis-related process in which Ca 2+ influx promotes muscle hyper-contraction. In contrast to mammals, DC is an early rather than a late event in C. elegans organismal death. Video Abstract [Figure presented] Galimov et al. describe mechanisms of organismal death in C. elegans. They document a rigor mortis-like wave of muscle hyper-contraction accompanied by Ca 2+ release and falling ATP, which is coupled to the previously described wave of intestinal necrosis in a process that resembles a distorted and deadly defecation cycle. ",
keywords = "ATP, C. elegans, aging, calcium, muscle, necrosis, organismal death, pathology, rigor mortis",
author = "Galimov, {Evgeniy R.} and Pryor, {Rosina E.} and Poole, {Sarah E.} and Alexandre Benedetto and Zachary Pincus and David Gems",
note = "Funding Information: We thank H. Imamura for providing the pRSETB-Queen-2m plasmid, P.E. Kuwabara for providing clp-1 strains, W.R. Schafer for providing the AQ2953 strain, M. Ezcurra for help with C. elegans strain construction, Y. Zhao for assistance with data analysis, A. Timpson, A. Dobson, and N. Alic for advice on statistical methodology, N. Stroustrup for useful discussion, and F. Cabreiro and H. Augustin for comments on the manuscript. This work was supported by a Wellcome Trust Strategic Award ( 098565/Z/12/Z ) and an EU grant ( FP6-518230 ) to D.G. Z.P. was supported by NIH grant R00AG042487 , Longer Life Foundation grant 2015-008 , and a Beckman Young Investigator award from the Arnold and Mabel Beckman Foundation . Some strains were provided by the Caenorhabditis Genetics Center, which is funded by NIH Office of Research Infrastructure Programs ( P40 OD010440 ). Funding Information: We thank H. Imamura for providing the pRSETB-Queen-2m plasmid, P.E. Kuwabara for providing clp-1 strains, W.R. Schafer for providing the AQ2953 strain, M. Ezcurra for help with C. elegans strain construction, Y. Zhao for assistance with data analysis, A. Timpson, A. Dobson, and N. Alic for advice on statistical methodology, N. Stroustrup for useful discussion, and F. Cabreiro and H. Augustin for comments on the manuscript. This work was supported by a Wellcome Trust Strategic Award (098565/Z/12/Z) and an EU grant (FP6-518230) to D.G. Z.P. was supported by NIH grant R00AG042487, Longer Life Foundation grant 2015-008, and a Beckman Young Investigator award from the Arnold and Mabel Beckman Foundation. Some strains were provided by the Caenorhabditis Genetics Center, which is funded by NIH Office of Research Infrastructure Programs (P40 OD010440). Publisher Copyright: {\textcopyright} 2018 The Author(s)",
year = "2018",
month = mar,
day = "6",
doi = "10.1016/j.celrep.2018.02.050",
language = "English",
volume = "22",
pages = "2730--2741",
journal = "Cell Reports",
issn = "2211-1247",
number = "10",
}